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A form of the protein capable of triggering this process can be conferred from one cell to another, thus inducing progressive neurodegeneration.
In addition, as BH3 profiling argued for the implication of mitochondria in mitotic cell death, we explored whether the pro-apoptotic Bax and/or Bak were required for triggering this process.
Although studies have shown that XO is present in human arterial and venous endothelial cells and can generate sufficient levels of oxygen radicals to trigger endothelial injury, questions remain regarding the role of xanthine and hypoxanthine formation in triggering this process.
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However, it is currently not known whether EMT contributes to airway remodeling in asthma and whether chronic allergic inflammation is sufficient to trigger this process.
These findings suggest that NPM/B23 is a direct target of Plk2 in the regulation of centriole duplication and that phosphorylation on serine 4 can trigger this process.
It takes place also in differentiating neuronal progenitors, where a surplus of Emx2OS-ncRNA is available to trigger this process (Fig. 5C, bottom left).
However, the progesterone and ZP3-induced acrosome reaction was not inhibited by capsazepine or BCTC, suggesting that TRPM8 activation triggers this process by a different signaling pathway.
Although the actual mechanism facilitating peroxisome acto-myosin interaction is not known, binding of RhoA-GTP to the peroxisomal membrane may trigger this process possibly by activating NMM IIA.
What triggers this process remains a matter of speculation.
Since the patient self-administered the ESAs, it is thinkable that an interrupted cold chain had triggered this process.
Thus, severe mitochondrial damage could trigger this process en masse, holding mitochondria within neuraxons and initiating neuroaxonal spheroid formation [ 31, 32 ▪ ].
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